SAH and Meningitis Flashcards

1
Q

What is the epidemiology of SAH ?
Sex ?
Age ?
Mortality rate ?

A

~6% of all strokes
▪ Slightly more females 1.6:1
▪ Most are under 50
▪ 50% mortality

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2
Q

What are risk factors for SAH ?

A
Hypertension
Smoking
 Excess alcohol consumption Predisposition to aneurysm formation
Family history
Trauma
Cocaine use
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3
Q

what are associated conditions for SAH ?

A

Chronic kidney disease (resultant effect on vessel
wall)
Marfan’s syndrome (effect on connective tissues of
vessels)
Neurofibromatosis (unclear mechanism, if any link)

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4
Q

What is the most common pathology for SAH ?

A

rupture of an aneurysm in the circle of Willis

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5
Q

What can cause aneurysm ?

A

genetic predisposition- absence of tunica media and lamina

haemodynamic effects at branch points in the circle of willis

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6
Q

what is the most common type of aneurysm in SAH?

A

Berry

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7
Q

list the most common site to least of Aneurysms for SAHs

A

30% - Anterior communicating artery proximal anterior
cerebral artery
Posterior communicating artery (25%)
Bifurcation of the middle cerebral artery as it splits
into superior and inferior divisions (20%)

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8
Q

what can be affected if Anterior communicating artery / proximal anterior
cerebral artery is affected in SAH ?

A

Can compress the nearby optic chiasm and

may affect frontal lobe or even pituitary

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9
Q

what can be affected if posterior

cerebral artery is affected in SAH ?

A

Can compress the adjacent oculomotor
nerve causing an ipsilateral third nerve
palsy

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10
Q

why do physiological changes happen in SAH ?

A

Bleeding into the subarachnoid space

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11
Q

what are early brain injury changes seen in SAH ? Why?

A

Microthrombi - these may occlude more distal branches
Vasoconstriction - Blood in CSF irritating arteries
Cerebral oedema - Inflammatory response to hypoxia
Apoptosis

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12
Q

what are cellular changes seen in SAH ?

A

Oxidative stress
Release inflammatory mediators - microglia
platelet activation

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13
Q

what are systemic complication of SAH ? what system is particularly activated ?

A

Sympathetic activation-
Early cushing response
Myocardial necrosis - sympathetic response
Inflammatory response

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14
Q

what is the headache seen in SAH ? describe what the patient will say

A
thunderclap 
onset is explosive and severe
worst headache I ve ever had 
diffuse pain 
lasts hours - wks
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15
Q

what other symptoms are present in SAH ?

A

LOC , Confusion , Dizzy, Meningism (Neck stiffness, photophobia ), focal neurology, history of sentinel bleed , cardiac arrest

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16
Q

What investigations need to be done in SAH ?

A

CT head
If confirmed = CT angiogram
Lumbar puncture

17
Q

what would CT look like in SAH ?

A

Prominent filling of the basal cisterns in a five pointed
‘star’ pattern
Blood may be seen within the ventricles (maybe due to
reflux from subarachnoid space)

18
Q

How would you undertake a lumbar puncture ?

A
  1. find iliac crest
  2. find L4/5
  3. insert needle between spinous process
  4. Feel give of lig flavum
  5. feel give of dura
  6. remove needle stylet and collect CSF
19
Q

what are LP findings in SAH ?

A

increased opening pressure
Bloody/ Xanthochromia
High protein
high red cell

20
Q

what is xanthochromia ?

A
yellow colouring of the
CSF due to metabolism of haemoglobin to
bilirubin within the subarachnoid space
 Seen at least 12 hours post bleed
More specific than frank blood for
SAH (helps exclude a
bloody/traumatic tap)
21
Q

what are LP findings in viral Meningitis ?

A

clear/cloudy appearance
Normal/ raised protein
High lymphocyte count

22
Q

what are LP findings in bacterial Meningitis ?

A

Cloudy
High protein
low glucose
high white cell = neutrophils

23
Q

what is treatment approach for SAH ?

A

ABC

support airway , give oxygen , fluid and nimodipine to alleviate cerebral vasospasm

24
Q

what in neuro obvs are you looking out for ?

A

signs of raised ICP

25
Q

what neruosurgcial options are their for SAH ?

A

Craniectomy - decompression
Coiling - platinum wire into the aneurysm = thrombosis of blood
clipping- spring clip around the neck of the
aneurysm, causing it to lose blood supply and
‘shrivel up’

26
Q

what are causative organisms in neonates for meningitis?

A

E. coli
Group B streptococcus
Listeria monocytogenes

27
Q

what are causative organisms in children for meningitis?

A

Haemophilus influenzae type B (HiB vaccine
given, ‘meningococcus’)
Neisseria meningitidis

28
Q

what are causative organisms in the elderly for meningitis?

A
Streptococcus pneumoniae (vaccines now given)
Listeria monocytogenes
29
Q

what are risk factors for meningitis ?

A
CSF defects (e.g. spina bifida)
Spina procedures (e.g. surgery, lumbar puncture)
Endocarditis (as a focus of bacteraemia)
Diabetes (immunosuppression)
Alcoholism
Splenectomy (immunosuppression)
Crowded housing (students at risk)
30
Q

what is the presentation of meningitis ?

A

Headache
• Neck stiffness (nuchal rigidity)
• Photophobia
with fever

31
Q

what are Associated symptoms of meningitis ?

A

Flu like symptoms, stiffness, photophobia, seizure, meningococcal rash (non- blanching), altered mental state, shock.
In babies- rigidity, bulging fontanelle, crying

32
Q

outline the pathophysiology of meningitis

A

Nasophyarngeal bacteria enter circulation
Bateramia = damage to vessel in the Brain and meninges = Enters SA space = Multiply in SA space .
Vasospasm = cerebral infarction
Inflammation = Increased CSF resistance = Hydrocephalus
increase BBB Pearmeabilty = Oedema = raised ICP
== decreased cerebral blood flow

33
Q

why is Maculopapular rash seen in meningococcal septicaemia?

A
microvascular thrombosis due to many
factors, including
Sluggish circulation
 Impaired fibrinolysis
Increased tissue factor expression in endothelial
cells
34
Q

what investigation to take for suspected Meningitis ?

A

bloods - cultures and PCR
Lumbar puncture
CT is non-resolving
Sepsis screen - CXR and MSU

35
Q

What is the supportive treatment for meningitis ?

A

Analgesia
• Antipyretics
• Fluids if shocked

36
Q

what is medical treatment of meningitis ?

A

IV ceftriaxone
• Dexamethasone to prevent hearing loss (due to swelling
of vestibulocochlear nerve or effect on cochlea)
if virial -
Aciclovir = herpes
Ganciclovir for CMV

37
Q

what are complications of Meningitis ?

A

Septic shock (due to bacteraemia)
Disseminated intravascular coagulation (due to bacteraemia)
Coma (due to raised ICP)
Cerebral oedema (due to cerebral inflammation)
Raised ICP
Death (due to brain herniation, sepsis)
SIADH (maybe direct effect on hypothalamus/pituitary?)
Seizures (due to irritation of brain parenchyma)
Hearing loss (due to swelling of vestibulocochlear nerve or
cochlea itself. Perilymph is continuous with subarachnoid
space)
Intellectual deficits (due to direct brain damage)
Hydrocephalus (due to interruption of CSF drainage pathways
and effect on arachnoid granulations)
Focal paralysis (maybe due to cerebral abscess)